香菇Latcripin-8蛋白诱导HepG-2细胞凋亡的 机制研究

目的探讨香菇Latcripin-8蛋白对HepG-2肝癌细胞凋亡的诱导作用及其机制。方法运用倒置显微镜、透射电镜、吉姆萨染色法和流式细胞仪法对细胞凋亡进行检测。采用Western blot法检测JAK3、STAT3和P53等凋亡相关蛋白的表达水平。采用Caspase-8活性检测盒检测Caspase-8活性。结果 HepG-2细胞经Latcripin-8蛋白作用后,倒置显微镜、透射电镜和吉姆萨染色等检测显示在形态学上Latcripin-8蛋白结构域抑制HepG-2细胞生长,并伴有凋亡小体产生。流式细胞仪检测显示该蛋白诱导HepG-2细胞凋亡。Western blot法检测结果显示JAK3和STAT3等蛋白的表达水平随药物浓度的增加而下降,而P53随药物浓度增加其表达量上升;凋亡相关因子Caspase-8的活性与对照组相比也均有不同程度的提高。结论香菇Latcripin-8蛋白结构域可能是通过JAK-STAT信号通路来诱导HepG-2肝癌细胞凋亡。

Latcripin-8 domain protein induced apoptosis in HepG-2 cells and its mechanisms

Abstract: Objective To explore whether apoptosis of HepG-2 cells can be induced by Latcripin-8 domain protein and its potential mechanism. Methods The apoptosis in HepG-2 cells was detected with inverted microscope, transmission electron microscope, Gimsa staining and flow cytometry. The expression of JAK3, STAT3 and P53 were determined with western blot method. Caspase Colorimetric assay kits were used to detect the activity of caspase-8. Results After treatment with Latcripin-8 domain protein, inverted microscope and transmission electron microscope displayed that the growth of HepG-2 cells was suppressed. Gimsa staining and flow cytometry showed that the protein induced the apoptosis of HepG-2 cells. The relative expression of protein P53 increased but the levels of JAK3 and STAT3 decreased along with the increase of the concentration of Latcripin-8. Compared to the control group, the activity of caspase-8 in Latcripin-8 group was increased. Conclusion Latcripin-8 domain protein can induce apoptosis in HepG-2 cells possibly through JAK-STAT pathway